A Mutation called D222G in a protein found in H1N1 virus may have caused many of the fatal and severe cases of virual pneumonia that occurred post H1N1 infection. According to a World Health Organisation report, the D222G mutation was found in less than two in every hundred cases of 2009 pandemic flu, but was responsible for around seven in every hundred deaths.
The new research shows that flu virus with the D222G mutation can bind to a broader range of receptors in the airway, including receptors that are present on cells called ciliated cells. These cells, found in the lining of the airway, have hair-like projections called cilia. The cilia sway back and forth to move mucus with trapped particles upward toward the mouth, and this is normally swallowed or coughed up. When ciliated cells become infected, the cilia stop moving and this vital clearance function is impaired. Inhaled viruses and bacteria can then reach the lung more easily, where they can potentially cause pneumonia.
The mutant virus has an increased capacity to infect ciliated cells, as shown by the collaborating group at the University of Marburg. Infection of the ciliated cells would sabotage the lungs’ clearing mechanism and could be one factor that made the D222G mutation more virulent, the researchers suggest.
The way scientists establish this is very interseting – Professor Feizi and her team study the receptor specificity of different flu viruses by attaching onto a glass surface a range of different carbohydrates, resembling the receptors present on the surface of airway lining cells. The virus is then incubated on top of the glass surface, and using a fluorescent dye, the researchers can see the receptors on the plate to which the virus binds.
This is an important finding not only because it can explain how the 2009 swine flu epidemic caused lung infection in select patients and that too in varying degrees of severity, but also it can provide scientists a way to study how the variants will affect future epidemics or pandamics. If D222G mutation is more widespread than in 2009 virus, it could have had devstating consequences along the lines of the 1918 pandemic. Understanding more about the virus and mutations like D222G better prepares us in combating.